Exercise Leads to Better Clinical Outcomes in Those Receiving Medication Plus Cognitive Behavioral Therapy for Major Depressive Disorder.

Joanne Gourgouvelis,Bernadette Ann Murphy,Hushyar Behbahani,Sandra T Clarke,Paul Yielder

doi:10.3389/fpsyt.2018.00037

Joanne Gourgouvelis, Bernadette Ann Murphy + Show 3 more

Open Access

https://doi.org/10.3389/fpsyt.2018.00037

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Abstract

The aim of this study is to investigate the effects of exercise as an add-on therapy with antidepressant medication and cognitive behavioral group therapy (CBGT) on treatment outcomes in low-active major depressive disorder (MDD) patients. We also explored whether exercise reduces the residual symptoms of depression, notably cognitive impairment and poor sleep quality, and aimed to identify putative biochemical markers related to treatment response. Sixteen low-active MDD patients were recruited from a mental health day treatment program at a local hospital. Eight medicated patients performed an 8-week exercise intervention in addition to CBGT, and eight medicated patients attended the CBGT only. Twenty-two low-active, healthy participants with no history of mental health illness were also recruited to provide normal healthy values for comparison. Results showed that exercise resulted in greater reduction in depression symptoms (p = 0.007, d = 2.06), with 75% of the patients showing either a therapeutic response or a complete remission of symptoms vs. 25% of those who did not exercise. In addition, exercise was associated with greater improvements in sleep quality (p = 0.046, d = 1.28) and cognitive function (p = 0.046, d = 1.08). The exercise group also had a significant increase in plasma brain-derived neurotrophic factor (BDNF), p = 0.003, d = 6.46, that was associated with improvements in depression scores (p = 0.002, R2 = 0.50) and sleep quality (p = 0.011, R2 = 0.38). We provide evidence that exercise as an add-on to conventional antidepressant therapies improved the efficacy of standard treatment interventions. Our results suggest that plasma BDNF levels and sleep quality appear to be good indicators of treatment response and potential biomarkers associated with the clinical recovery of MDD.

Highlights

Major depressive disorder (MDD) is a global public health problem being the second leading cause of disability worldwide [1, 2] and projected to be the leading cause by 2030 [2]
The MDD group was significantly older than the healthy group, t(36) = 12.31, p < 0.0001, given that we intentionally recruited younger individuals to provide normative data for comparison from healthy individuals with no history of mental health illness or other confounding pathologies that increase with age
Cognitive tests revealed that the MDD group performed significantly poorer on the Montreal Cognitive Assessment (MoCA), t(36) = 2.32, p = 0.026; had significantly more errors for the Paired Associates Learning (PAL) test, t(35) = 3.90, p = 0.0004; and had a significantly longer correct response latency for the delayed matching to sample (DMS) test t(35) = 2.44, p = 0.020, suggesting cognitive impairment

Summary

Introduction

Major depressive disorder (MDD) is a global public health problem being the second leading cause of disability worldwide [1, 2] and projected to be the leading cause by 2030 [2]. Over 40% of MDD patients who are considered in partial or full remission continue to experience residual symptoms and are at greater risk for relapse, highlighting the need for more efficacious antidepressant therapies [10, 11]. The etiology and pathogenesis of MDD is thought to be multifaceted, making it very challenging for researchers to develop novel efficacious antidepressant therapies. People with MDD have consistently been found to have reduced hippocampal volumes [13,14,15] and impaired hippocampal function during memory encoding and retrieval processes [16,17,18,19,20]

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